Cardiac muscle is an involuntary, striated muscle. Cardiac muscle cells are relatively small (10 µm × 100 µm) and form an electrical syncytium with tight electrical and mechanical connections between adjacent cardiac muscle cells. Action potentials are initiated in the sinoatrial node and spread quickly throughout the heart to allow synchronous contraction, a feature important for the pumping action of the heart.
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Contraction of cardiac muscle involves the Ca++dependent interaction of actin and myosin filaments, as in skeletal muscle. However, unlike skeletal muscle, cardiac muscle requires an influx of extracellular Ca++ . Specifically, the influx of Ca++ during an action potential triggers release of Ca++ from the SR, which then promotes actin-myosin interaction and contraction.
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Relaxation of cardiac muscle involves reaccumulation of Ca++ by the SR and extrusion of Ca++ from the cell via the 3Na+-Ca++ antiporter and the sarcolemmal Ca++ pump. The Ca++ pump of the SR is associated with numerous proteins (forming a regulosome), including some endogenous micropeptide inhibitors and activators.
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The force of contraction of cardiac muscle is increased by stretch (Frank-Starling Law of the Heart) and by sympathetic stimulation. Skeletal muscle, in contrast, increases force by recruiting more muscle fibers or by tetany.
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Hypertrophy of the heart can occur in response to exercise, chronic pressure overload, or genetic mutations. The cardiac hypertrophy resulting from exercise is typically beneficial, with improved cardiac performance, increased oxygen consumption, and normal relaxation. Chronic pressure overload, on the other hand, can result in cardiac hypertrophy that is initially associated with a decreased β-adrenergic response but may progress to dilated cardiac hypertrophy, characterized by decreased contractile ability. Genetic mutations resulting in cardiac hypertrophy include familial hypertrophic
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cardiomyopathy, in which a mutation in a single intracellular protein may alter contractile function and promote a hypertrophic response. Researchers have identified a microRNA that appears to contribute to the exercise-induced hypertrophy of the heart and to inhibit maladaptide remodeling after ischemia/reperfusion injury.
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